2. Objectives
⢠Whatâs Bicarbonate
⢠How it works
⢠Dose ?
⢠How can we give it
⢠Contraindications and Safety
⢠Who do you want to give it?
⢠When shall we use it
⢠Bicarbonate Disadvantages
⢠Bicarbonate Alternatives
4. Whatâs Sodium Biacarbonate ?
⢠IV fluid with pH of 8.0
⢠8.4% solution contains 1 mEq/mL of NaHCO3
and is very hypertonic (2,000mOsm/kg)
⢠7.5% solution contains 0.9 mEq/mL of NaHCO3
⢠4.2% solution contains 0.5 mEq/mL of NaHCO3
7. ⢠One Ampule of bicarbonate fully reacted will
generate over 11 of CO2 and 1.5 meq/L of Hco3
⢠Resp Acidosis, So what ?
Current Opinion in Critical Care 2008, 14:379â383
8. ⢠Respiratory Acidosis Decreases left ventricular
contractility but increased overall CO by 23%
due to decrease SVR and increase HR
Circultion Research 1990;67:628-635
11. Dose
⢠Based on the calculated Deficit :
⢠HCO3
-(mEq) = 0.5 x weight (kg) x [24 - serum
HCO3
-(mEq/L)]
⢠Administer 1/2 dose over 3-4 hrs, then
remaining 1/2 dose over the next 24 hours;
12. ⢠If acid-base status is not available: 2-5 mEq/kg
I.V. infusion over 4-8 hours; subsequent doses
should be based on patient's acid-base status
⢠initial goal of therapy is to target a pH of ~7.2
and a HCO3
- of ~10 mEq/L to prevent
overalkalinization.
16. No Hco3 Bolus
⢠IV-push administration should be reserved for
cardiac life support whenever indicated and not
metabolic acidosis
Koda-Kimble M, Young LY, et al. Handbook of Applied Therapeutics. Lippincott Williams & Wilkins, 2006. P10.3(1104)
18. Safety
⢠Pregnancy Risk Factor C
⢠Breast-Feeding Considerations Sodium is
found in breast milk
⢠Still No Enough Data !!
â˘Do you Really Care ?
19.
20. Extravasation management
⢠Stop infusion immediately and disconnect (leave
cannula in place); gently aspirate extravasated
solution (do NOT flush the line); initiate
hyaluronidase antidote; remove cannula;
apply dry cold compresses elevate extremity.
⢠Hyaluronidase: SubQ: Inject four to five
separate 0.2 mL injections of 15 units/mL
around area of extravasation (Hurst, 2004).
Dimens Crit Care Nurs. 2004 May-Jun;23(3):125-8
21. Potential harms of bicarbonate
therapy
⢠Increased PCO2
⢠Hypernatremia
⢠Extracellular fluid (ECF) volume expansion
⢠Intracellular and CSF Acidosis (CO2)
⢠Hypokalemia
⢠severe tissue necrosis if extravasation takes
place
⢠rebound alkalosis
Ann Intern Med. 1986;105(6):836
Diabetes 1974, 23:405-411
N Engl J Med 1971, 284:283-290
22. ⢠bicarbonate increases lactate production by:
⢠increasing the activity of the rate limiting
enzyme phosphofructokinase and removal of
acidotic inhibition of glycolysis
⢠shifts Hb-O2 dissociation curve, increased
oxygen affinity of haemoglobin and thereby
decreases oxygen delivery to tissues
⢠hyperosmolality (cause arterial vasodilation and
hypotension)
23. ⢠Reduced ionized calcium by 10% (10% drop may
decrease cardiac and vascular contractility and
responsiveness to catecholamines)
Ann Intern Med. 1990;112(7):492-498
24. Before you Give Bicarb :
⢠Correct the underlying cause of acidosis and give
supportive care
⢠Ensure adequate ventilation to eliminate CO2
⢠Correct hypoxia
⢠Think twice before you give it in high anion gap
acidosis
26. Why do you want to give bicarb ?
⢠What are the deleterious effects of acidemia, and
when are they manifest?
⢠When is acidemia severe enough to warrant
therapy?
27. Why do you want to give bicarb ?
⢠metabolic acidosis leads to adverse
cardiovascular effects:
⢠Reduced left ventricular contractility
⢠Arrhythmias
⢠Arterial vasodilation and venoconstriction
⢠Impaired responsiveness to catecholamine
vasopressors
30. Does bicarbonate improve
management of severe DKA ?
⢠Ann Pharmacother. 2013 Jul-Aug;47(7-8):970-
5:
⢠Intravenous bicarbonate therapy did not
decrease time to resolution of acidosis or
time to hospital discharge for patients with
DKA with an initial pH <7.0.
31. ⢠Crit Care Med. 1999 Dec;27(12):2690-3:
⢠Not in favor of the use of bicarbonate in the
treatment of diabetic ketoacidosis with pH
values between 6.90 and 7.10.
32. ⢠Ann Intern Med 1986;105:836â840:
⢠administration of bicarbonateto pt with pH
(6.9 to 7.14) does not affect recovery outcome
variables as compared with those in a control
group.
33. In Pediatrics
⢠Ann Emerg Med. 1998. Jan;31 (1):41-8.:
⢠Prolonged hospitalizations were noted in the
bicarbonate group
⢠No evidence that adjunctive bicarbonate
improved clinical outcome in children with
severe DKA (pH < 7.15).
⢠The rate of metabolic recovery and
complications were similar in patients
treated with and without bicarbonate
34. Systematic review of 44 studies :
⢠Ann Intensive Care. 2011 Jul 6;1(1):23
⢠Showed increased risk for cerebral edema and
prolonged hospitalization in children who
received bicarbonate, and weak evidence of
transient paradoxical worsening of ketosis, and
increased need for potassium supplementation
35. Bicarb Increases Ketosis :
⢠Br Med J (Clin Res Ed). 1984 October 20; 289(6451):
1035â1038.
slower rate of lactate clearance, implying
impaired tissue oxygenation
⢠J Clin Endocrinol Metab. 1996 Jan;81(1):314-20
The group receiving NaHCO3 showed a 6-h
delay in the improvement of ketosis as
compared with controls
36. Cerebral Edema in Pediatrics
⢠N Engl J Med 2001;344:264â269
⢠cerebral edema occurs in approximately 1%
of episodes of DKA in children with a
mortality rate of 40-90%
⢠only treatment with bicarbonate was
associated with cerebral edema
37. Cerebral Edema Risk Factors
⢠Use of bicarbonate
⢠Younger age
⢠newly diagnosed diabetes
⢠hypocapnia
⢠Severe acidosis
⢠higher serum glucose, urea nitrogen, and
creatinine concentrations at the time of
presentation
N Engl J Med. 2001;344(4):264
J Pediatr. 1980;96(6):968
38. Conclusion
⢠Do not use NaHCO3 routinely in the
management of DKA
⢠Despite the lack of evidence many intensivists
have a personal cut-off pH at which they
consider giving HCO3- in severe acidemia due to
DKA (typically < pH 6.9 to 7.0) as a âlast ditchâ
measure
39. Ann Intern Med. 1987;106(4):615
⢠To be used in collapsing pt.
1) patients with a pH <7.0, in whom decreased
cardiac contractility and vasodilatation may
be impairing tissue perfusion
2) patients with severe hyperkalemia
3) patients with coma
40. If you want to give it
⢠patients with a pH <6.9, 100 meq of Hco3 in
400 mL sterile water at a rate of 200 ml/h.
⢠pH of 6.9â7.0, 50 mmol sodium bicarbonate
is diluted in 200 ml sterile water and infused at
a rate of 200 ml/h.
⢠No bicarbonate is necessary if pH is >7.0
Diabetes Care January 2004 vol. 27 no. suppl 1 s94-s102
41. American Diabetic Association (ADA)
⢠Says bicarbonate âmay be consideredâ in
patients with pH < 6.9 in DKA
⢠High level evidence is lacking !!
42.
43. Lactic Acidosis
⢠the most common cause of metabolic acidosis in
hospitalized patients
⢠Type A :due to marked tissue hypoperfusion in
shock
⢠Type B : toxin-induced impairment of cellular
metabolism
⢠Metformin
⢠Alcoholism
⢠Malignancy
⢠HIV infection
44. D-lactic acidosis
⢠rare form of lactic acidosis that can occur in
patients with short bowel syndrome or other
forms of gastrointestinal malabsorption who
ingest large amount of carbohydrates
⢠Ingestion of propylene glycol
⢠Some DKA Patients
45. Lactic Acidosis
⢠Lactic Acidosis that is severe enough to warrants
Bicarb therapy already has a high mortality to
begin with
⢠Literature Review done :
⢠Chest. 2000 Jan;117(1):260-7
⢠we do not give or advise bicarbonate
infusion regardless of the pH.
46. Uptodate
⢠suggest that patients with lactic acidosis and
severe acidemia (pH <7.1 and Hco3 below or
equal to 6 meq/L ) receive bicarbonate therapy
(tube the pt. if PCo2 >20 for Inadequate
ventilation)
47. Review Article
⢠In view of the paucity of data, we are not able to
agree or disagree with Bicarb treatment
⢠we do not think that bicarbonate administration
is indicated for LA due to shock if pH > 7.0
Current Opinion in Critical Care 2008, 14:379â383
48. ⢠in hemorrhegic lactic acidosis on animal study
Bicarbonate treatment along with
hyperventilation and calcium administration
increases pH and improves cardiovascular
function
Anesthesiology. 2013 Nov 20
49. Bicarb and Mortality
⢠Sodium bicarbonate administration was an
independent factor associated with higher
mortality
PLoS One. 2013 Jun 5;8(6):e65283
50. ⢠Sodium bicarbonate elevated blood lactate
concentrations to a greater extent than did either
sodium chloride or no treatment.
Science 15 February 1985
51. prospective randomized, double-blind,
controlled clinical trial
⢠I: in first stage sodium bicarbonate was given by
venous drip until pHâĽ7.15, and in second stage
sodium bicarbonate was given by intravenous
drip till pHâĽ7.25 after 6 hours
⢠C: intravenous drip of sodium bicarbonate was
used till pHâĽ7.15
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Jan;25(1):24-7
52. Their conclusion !!
⢠The use of sodium bicarbonate in stages in
treating hypoperfusion induced lactic acidemia
as a result of septic shock can lower the
occurrence rate of multiple organ dysfunction
syndrome, time of mechanical ventilation,
durations of stay in ICU and in hospital, and
mortality
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Jan;25(1):24-7
53. Surviving Sepsis Campaign 2012
⢠We recommend against the use of sodium
bicarbonate therapy for the purpose of
improving hemodynamics or reducing
vasopressor requirements in patients with
hypoperfusion-induced lactic acidemia with pH
⼠7.15 (grade 2B).
⢠No good Evidence on pH< 7.15
54. PH>7.1
⢠Two randomized trials failed to find a benefit of
bicarbonate therapy in critically ill patients with
lactic acidosis and pH values > 7.1
55. Prospective, randomized, blinded,
crossover study
⢠Correction of acidemia using sodium
bicarbonate does not improve hemodynamics in
critically ill patients who have metabolic acidosis
and increased blood lactate
⢠pH (from 7.22 to 7.36) and serum bicarbonate
(from 12 to 18 mmol/L)
Ann Intern Med. 1990 Apr 1;112(7):492-8.
56. Prospective, randomized, blinded,
crossover study
⢠Bicarbonate therapy significantly increased the
arterial pH (from 7.16 to 7.21) and serum
bicarbonate (from 16 to 19 mmol/L)
⢠The infusion of sodium bicarbonate and sodium
chloride produced similar changes in cardiac
output, mean arterial pressure, and pulmonary
artery pressure
⢠Improving Numbers not M&M
Ann Intern Med. 1990 Apr 1;112(7):492-8.
57. Prospective, randomized, blinded,
crossover study
⢠Administration of sodium bicarbonate did not
improve hemodynamic variables in patients with
lactic acidosis, but did not worsen tissue
oxygenation.
Crit Care Med. 1991 Nov;19(11):1352-6
58. Case Report
⢠43-year-old woman K/c HTN on atenolol and
Anxiety on Mirtazipine and lorazepam was
brought to the hospital with chest pain for 20
hours radiating to her Back
⢠Temp 32.5C BP 66/45 mmHg HR 57
⢠Denied Hx of Ingestion
⢠Tx as Septic Shock due to pneumonia
⢠4 hrs later her condition deteriorated, Got tubed
Case Reports in Nephrology Volume 2012 (2012), Article ID 671595
59. ⢠pH 6.56, bicarbonate 3 mmol/L, and lactate
18.4 mmol/L
⢠AG 31
⢠serum creatinine of 162 Οmol/L with a serum
potassium of 5.3 mmol/L
⢠Hco3 Infusion Started
⢠NE, Dobutamine, phenylephrine and
Vassopressin Started
Case Reports in Nephrology Volume 2012 (2012), Article ID 671595
60. ⢠PAN CT and TEE was Done INCONCLUSIVE for
aortic disease
⢠A Nurse Calling you for K+ 7.8 and GC
1.2mmol/l
⢠AG 43
⢠Urine Tox Positive for Benzo and opioid
⢠Serum tox Acetaminophen level 81¾mol/L
⢠Chart Arrived and shows a suicidal attempt 15
years ago by overdose
Case Reports in Nephrology Volume 2012 (2012), Article ID 671595
61. ⢠A member of the family revealed that she have
DM and on metformin
⢠Metformin Level 170¾g/mL (therapeutic range
1-2Âľg/mL)
⢠CRRT Started
⢠THAM, 0.3 mmol/L, 36 mg/mL, 1600 mg
administered by infusion at 300 mL/hr for 5
hours
Case Reports in Nephrology Volume 2012 (2012), Article ID 671595
62. 90 mg Metformin !!
⢠Afterward Pt improved, Extubated Admitted
Taking 90 mg Metformin
Case Reports in Nephrology Volume 2012 (2012), Article ID 671595
63. Metformin Toxicity
⢠Dtsch Med Wochenschr. 2000 Mar
3;125(9):249-51
⢠Conventional management of the lactic acidosis
neither corrected the acidosis nor stabilized the
circulatory system. Continuous veno-venous
haemodialysis with bicarbonate-buffered
solutions succeeded in reducing the need for
catecholamines
64. Metformin Toxicity
⢠Diabetes Care June 1999 vol. 22 no. 6 925-927
⢠9 per 100,000 person-years
⢠Biguanides and NIDDM.Diabetes Care 15:755â
772, 1992
⢠Metformin. N Engl J Med 334:574â579, 1996
⢠The lactic acidosis rate in metformin
users has been reported to be much lower: 0â
8.4 cases per 100,000 person-years
65. Risk factors
⢠age of >60 yr
⢠decreased cardiac
⢠Hepatic Disease
⢠renal function
⢠diabetic ketoacidosis
⢠surgery
⢠respiratory failure
⢠ethanol intoxication
⢠fasting
66. Severe acidosis in Trauma
⢠retrospective therapeutic cohort study of 225
severely acidotic (arterial pH ⤠7.10) between
1989-2011
⢠if dead space in the lungs increases due to shock
with poor lung perfusion, the arterial-end tidal
PCO2 difference [P(a-ET)CO2] increases
J Trauma Acute Care Surg. 2013 Jan;74(1):45-50
67. ⢠2-8 vials of HCO3 given
⢠HCO3 10.5 (3.1) to 16.8 (4.0) mEq/L
⢠PaCO2 44 (9) to 51 (11) mmHg
⢠end-tidal CO2 stayed relatively constant 26 [6] to
25 [5]
⢠P(a-ET)CO2 from 17 (9) to 24 (13) mmHg
⢠More Dead Space !
J Trauma Acute Care Surg. 2013 Jan;74(1):45-50
68. ⢠75 patients who survived had P(a-ET)CO2 10 (6)
mm Hg
⢠103 patients who died in the operating room or
within 48 hours of surgery had a P(a-ET)CO2 of
23 (10) mm Hg
J Trauma Acute Care Surg. 2013 Jan;74(1):45-50
69. ⢠We have found that in severely injured patients,
P(a-ET)CO2 of less than 10 mm Hg is associated
with survival and P(a-ET)CO2 of greater than 16
mm Hg is usually fatal.
⢠Our initial studies suggested that intravenously
administered bicarbonate increases P(a-ET)CO2
J Trauma Acute Care Surg. 2013 Jan;74(1):45-50
70. Sodium bicarbonate supplements for
treating acute kidney injury
⢠Cochrane Review was Done 2012
⢠We did not find any randomized controlled trials
(RCTs) that assessed the benefits or harms of
giving sodium bicarbonate to people with acute
kidney problems.
71. Bicarb is not that good !
⢠Tromethamine (THAM)
⢠Carbicarb
⢠Dichloroacetate (DCA)
⢠CRRT
72. Carbicarb
⢠is a mixture of Na2CO3/NaHCO3 that buffers
similarly to NaHCO3, but without net generation
of CO2
⢠Same risks of hypertonicity and hypervolemia
are similar to those of sodium bicarbonate
73. Comparing carbicarb Vs.bicarb in
hypoxic LA
⢠28 Dogs with HLA Given 2.5 meq/kg of either
NaHCO3 or carbicarb over 1 hr.
⢠Lactate use by muscle, gut, and liver all
improved with carbicarb and decreased with
NaHCO3.
Circulation 77, No. 1, 227-233, 1988
Carbicarb Bicarb
PH (7.22 to 7.27 7.18 to 7.13
PCo2 No Change
Lactate Stabilized
74. ⢠Twenty-one dogs were anesthetized,
mechanically ventilated, and randomly allocated
into:
⢠Carbicarb
⢠sodium bicarbonate
⢠sodium chloride
⢠Carbicarb administration in HLA improved
hemodynamics compared with sodium
bicarbonate or sodium chloride administration
Chest. 1993;104(3):913-918
75. THAM
⢠A biologically inert amino alcohol of low toxicity,
which buffers H+ and gets excreted in the urine
without production of Co2
⢠Administration of THAM in ALI cases was
associated with significant improvements in
arterial pH and base deficit, and a decrease in
arterial carbon dioxide tension
⢠Toxicities of THAM include hyperkalemia,
hypoglycemia, and respiratory depression
Am J Respir Crit Care Med. 2000 Apr;161(4 Pt 1):1149-53
76. Bicarb + THAM
⢠Using a blood-perfused isolated heart
preparation, left ventricular contractility and
relaxation were measured
⢠The combination of THAM with NaHco3 is
based on the ability of THAM to capture the CO2
produced by the sodium bicarbonate buffer. This
combination achieves a perfect correction of
metabolic acidosis and improves myocardial
performance.
Am J Respir Crit Care Med. 1997 Mar;155(3):957-63
77. CRRT
⢠Use bicarbonate-based replacement fluid over
citrate as citrate may increase the strong ion gap
Current Opinion in Critical Care 2008, 14:379â383
78. When shall we use it
⢠Accepted
⢠Hyperkalaemia
⢠Treatment of sodium channel blocker
overdose (e.g. tricyclic overdose)
⢠Urinary alkalinisation (salicylate poisoning)
⢠Metabolic acidosis (NAGMA) due to HCO3
loss (RTA, fistula losses)
79. ⢠Controversial
⢠Diabetic ketoacidosis (very rarely, perhaps if
shocked and pH < 6.8)
⢠Severe pulmonary hypertension with RVF to
optimize RV function
⢠Severe ischemic heart disease where lactic
acidosis is thought to be an arrhythmogenic
risk
80. Cardiac Arrest
⢠The empirical early administration of sodium
bicarbonate (1 mEq/kg) has no effect on the
overall outcome in prehospital cardiac arrest.
However, a trend toward improvement in
prolonged (>15 minutes) arrest outcome was
noted.
⢠2-fold increase in survival (32.8% vs 15.4%) !
Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest Am J Emerg Med. 2006;24(2):156
81. ⢠retrospective cohort
⢠The administration of sodium bicarbonate at
around 36 Minutes of CPR did not signiďŹcantly
improve the rate of ROSC in out-of-hospital
cardiac arrest
American Journal of Emergency Medicine 31 (2013) 562â565
82. No Benifit
⢠Buffer therapy during out-of-hospital
cardiopulmonary resuscitation. Resuscitation. 1995;29:89
â95. (RCT)
⢠Sodium bicarbonate improves outcome in pro-
longed prehospital cardiac arrest. Am J Emerg Med.
2006;24:156 â161.
⢠Prehospital bicarbonate use in cardiac arrest: a
3-year experience. Am J Emerg Med. 1992;10:4 â7.
83. ⢠Out-of-hospital buffer therapy in heart arrest
Tidsskrift for den Norske Laegeforening : Tidsskrift for Praktisk Medicin,
ny Raekke [1996, 116(27):3212-3214
85. ACLS Guidelines 2010
⢠Giving sodium bicarbonate during CPR is not
helpful and may even be harmful!
⢠(Class III, LOE B).
86. ⢠Bicarbonate may compromise CPR by reducing SVR
⢠It can create extracellular alkalosis that will shift the
oxyhemoglobin saturation curve and inhibit oxygen
release.
⢠It can produce hypernatremia and therefore
hypersmolarity.
⢠It produces excess CO2, which freely diffuses into
myocardial and cerebral cells and may paradoxically
contribute to intracellular acidosis.
⢠It can exacerbate central venuous acidosis and may
inactivate simultaneously administered
catecholamines.
87. ⢠prospective, randomized, double-blind,
controlled trial
⢠36% receiving buffer were admitted to hospital
ICU and (10%) were discharged from hospital
alive, vs. (36%) and (14%) receiving saline
Buffer therapy during out-of-hospital cardiopulmonary resuscitation Resuscitation. 1995;29(2):89
88. Hyperkalemia
⢠Though no studies demonstrate harm, the solo
administration of bicarbonate does not acutely
decrease potassium levels. But it may improve
insulin/albuterol action on potassium in acidotic
patients.
⢠Donât Give It Alone
⢠If you want to Give it Give as infusion (150mEq
in 1 liter D5%)
Miner Electrolyte Metab. 1991;17(5):297 Kidney Int. 1992;41(2):369
89. Rhabdomyolisis
⢠There is no evidence that bicarbonate is helpful
or harmful in rhabdomyolysis
⢠An excellent EBMedicine.net
review recommends bicarbonate if urine pH
<6.5 with CK level > 5000 as class III evidence â
indicating âit may be acceptable, possibly useful,
considered optional or an alternative treatment
90. bicarbonate is still recommended in
⢠TCA overdose
⢠Salicylate toxicity
⢠Phenobarbarbital
⢠Chlorpropamide
⢠Chlorophenoxy herbicide poisoning
⢠Cocaine overdose
⢠Organophosphate poisoning
⢠Methanol and ethylene glycol
⢠Increased ICP
91. Home Message
⢠Bicarbonate has many complication you have to
be aware of
⢠In NAGMA (Absolute bicarb loss) give it with no
doubt aiming for Hco3 20
⢠There are other options to Hco3
⢠Its usually a last resort choice after treating the
underlying disease
Acute respiratory acidosis decreases left ventricular contractility but increases cardiacoutput in dogs
Dimens Crit Care Nurs. 2004 May-Jun;23(3):125-8
Ann Intern Med. 1986;105(6):836
Diabetes 1974, 23:405-411
N Engl J Med 1971, 284:283-290
HCO3 may cause clinical deterioration if tissue hypoxia present due to removal of acidotic inhibition of glycolysis and leftward shift of the oxy-Hb dissociation curve
(lactate and ketoacidosis â organic acids are metabolised thus regenerating HCO3
correct underlying cause of acidosis and give supportive care
The use of bicarbonate might help close the anion gap, but may simultaneously delay correction of the acidosis (low HCO3). This occurs because, while ketones are excreted in the urine, they are naturally excreted with an equal amount of protons when they are excreted with hydrogen or ammonium. Meanwhile, some of the ketoacids will be metabolized to regenerate some of the lost HCO3. This process both closes the anion gap and corrects the acidosis. On the other hand, when bicarbonate is used ketones are excreted with sodium and potassium, which are considered bicarbonate precursors. This process leads to a paradoxical loss of potential bicarbonate, as well as a hyperchloremic non-anion-gap metabolic acidosis. Interestingly, this does not happen in ESRD patients, since they cannot excrete excessive amounts of urinary ketones and bicarbonate precursors
Alkali administration can lead to a posttreatment metabolic alkalosis, since metabolism of ketoacid anions with insulin results in the generation of bicarbonate and spontaneous correction of most of the metabolic acidosis
metabolized by bacteria in the colon to D-lactic acid, which is then absorbed into the systemic circulation
(Lactobacilli)
Chest. 2000 Jan;117(1):260-7
Anesthesiology. 2013 Nov 20
(PLoS One. 2013 Jun 5;8(6):e65283)
Science 15 February 1985
Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Jan;25(1):24-7
Ann Intern Med. 1990 Apr 1;112(7):492-8.
Crit Care Med. 1991 Nov;19(11):1352-6
Metformin-Associated Lactic Acidosis following Intentional Overdose Successfully Treated with Tris-Hydroxymethyl Aminomethane and Renal Replacement Therapy
Case Reports in Nephrology
Volume 2012, Article ID 671595, 5 pages
doi:10.1155/2012/671595
Incidence of lactic acidosis in metformin users.
J Trauma Acute Care Surg. 2013 Jan;74(1):45-50
Carbicarb is a mixture of Na2CO3/NaHCO3 that buffers similarly to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% O2/92% N2). Dogs with HLA (n = 28) were then treated with 2.5 meq/kg of either NaHCO3 or carbicarb over 1 hr. Measurements were made, after 1 hr of hypoxia and 1 hr of therapy, of: cardiac hemodynamics, blood gases, liver intracellular pH (pHi), oxygen consumption, and regional lactate production. After therapy, the arterial pH rose with carbicarb (7.22 to 7.27, p less than .01), and fell with NaHCO3 (7.18 to 7.13, p less than .01). Mixed venous PCO2 did not change with carbicarb but increased with NaHCO3 (p less than .05). Arterial lactates stabilized with carbicarb but rose with NaHCO3 (by 3.1 mmol/liter, p less than .005). Lactate use by muscle, gut, and liver all improved with carbicarb and decreased with NaHCO3. The liver pHi (normal = 6.99, hypoxia = 6.80) improved with carbicarb (to 6.92), but decreased further with NaHCO3 (to 6.40). Muscle O2 consumption rose with carbicarb, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (-12 vs -46 mm Hg, p less than .006) and the cardiac output was stable with carbicarb but decreased with NaHCO3 (from 143 to 98 ml/kg/min, p less than .004). Stroke volume also improved with carbicarb but therewas no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility
Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis
Circulation 77, No. 1, 227-233, 1988.
Chest. 1993;104(3):913-918
Mechanical hyperventilation of acidemic patients with acute lung injury (ALI) requires the use of high volumes and pressures that may worsen lung injury. However, permissive hypercapnia in the presence of shock, metabolic acidosis, and multi-organ system dysfunction may compromise normal cellular function. Tris-hydroxymethyl aminomethane (THAM) may be an effective method to control acidosis in this circumstance. Protonated THAM is excreted by the kidneys, so that carbon dioxide production is not raised. In an uncontrolled study, we administered THAM to 10 patients with acidosis (mean pH = 7.14) and ALI (mean lung injury score = 3.28) in whom adequate control of arterial pH could not be maintained during either eucapnic ventilation or permissive hypercapnia ventilation. THAM was given at a mean dose of 0.55 mmol/kg/h. Administration of THAM was associated with significant improvements in arterial pH and base deficit, and a decrease in arterial carbon dioxide tension that could not be fully accounted for by ventilation. Although further studies are needed to confirm these observations, THAM appears to be an effective alternative to sodium bicarbonate for treating acidosis during ALI.
Am J Respir Crit Care Med. 2000 Apr;161(4 Pt 1):1149-53
Am J Respir Crit Care Med. 1997 Mar;155(3):957-63
Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest
Am J Emerg Med. 2006;24(2):156
Buffer therapy during out-of-hospital cardiopulmonary resuscitation
Resuscitation. 1995;29(2):89
The purpose of the study was to evaluate the potassium-lowering effect of hypertonic versus isotonic sodium bicarbonate (NaHCO3) in patients with end-stage renal disease (ESRD) receiving chronic maintenance hemodialysis. Immediately prior to dialysis, we infused isotonic (1.4%, 150 mEq/l) NaHCO3 in H2O (1 mEq/kg body weight over 2 h) to 10 patients with ESRD. Blood was drawn in heparinized tubes, without the use of a tourniquet, from the angioaccess for Na, K, pH, PCO2, HCO3, and osmolality at baseline (x 3) and after 10, 20, 40, 60, 90, 120, and 180 min of infusion. All patients were acidotic (HCO3 13-21 mEq/l, pH 7.25-7.38) prior to the study. In these patients, plasma HCO3 increased by an average of 3 mEq/l, and plasma K decreased by 0.35 mEq/l at 180 min. Plasma osmolality did not change. In 8 patients, a bolus of hypertonic (8.4%, 1,000 mEq/l) NaHCO3 (1 mEq/kg body weight over 5 min) tended to cause a transient increase in plasma HCO3, an increase in plasma osmolality, and minor changes in the K levels (an initial small and transient albeit significant decrease, followed by a tendency to increase). Finally, plasma K tended to increase in patients receiving infusions of either isotonic (n = 6) or hypertonic (n = 6) sodium chloride. Our data do not support the efficacy of the common practice of administering NaHCO3 for the emergency treatment of hyperkalemia in patients with ESRD receiving maintenance dialysis.
Miner Electrolyte Metab. 1991;17(5):297
Effect of prolonged bicarbonate administration on plasma potassium in terminal renal failure
Kidney Int. 1992;41(2):369